According to foreign media BGR reports,Five critical genetic differences between the chd-2700 patients and the UK population that may lead to serious genetic problems from the study.This breakthrough could lead to the discovery of new therapies that specifically target the types of genetic imbalances that can lead to life-threatening complications. The genetic problems they found included genes involved in antiviral immunity and lung inflammation.
Researchers at the Roslin Institute at the University of Edinburgh have just released a breakthrough coronavirus study that explains why some patients develop severe covid-19 cases. Researchers recently explained that interferon related gene imbalances may increase the risk of complications in young patients who are not expected to develop into severe cases of covid-19. These genetic problems persist and are not the result of covid-19 infection. But no other disease brings them to the surface.
It has been proved that it is not only the genes controlling interferon that can affect the prognosis of covid-19. Interferon is a protein that is part of the immediate immune response after infection with pathogens. Roslin researchers studied the DNA of 2700 critically ill patients with covid-19 in the UK and identified five genetic problems that could lead to a more dangerous version of the disease. The finding could lead to new treatments, as doctors reuse drugs currently available to deal with these particular genetic problems.
The genomic consortium researchers compared the genetic information of 2700 ICU patients with samples of healthy volunteers in other studies. They found key differences in these five genes. IFNAR2, Tyk2, OAS1, DPP9 and CCR. They "partly explain why some covid-19 patients get worse, while others are unaffected," the researchers said.
"Our findings reveal that critical illness of covid-19 is associated with at least two biological mechanisms: congenital antiviral defense, which is an important mechanism known in the early stage of the disease (IFNAR2 and OAS genes), and host driven inflammatory lung injury, which is the key mechanism of late life-threatening covid-19 (DPP9, Tyk2 and CCR2)," the researchers wrote.
"This is an amazing realization of the commitment of human genetics to help understand critical illness," Dr. Kenneth Baillie, the project's lead researcher, said in a statement. "Our results immediately highlight which drugs should be at the top of the list of clinical trials. We can only test a few drugs at a time, so making the right choice will save thousands of lives. "
Researchers can predict what kind of drugs will work in critically ill patients with covid-19. They found that lowering the activity of the Tyk2 gene could protect the disease. Anti inflammatory drugs from a group called JAK inhibitors may help. An example of this drug is barictinib.
Another finding involved the infar2 gene. Increasing the activity of the gene can create protection because it will mimic the effect of interferon therapy. But this treatment should be used early in the infection to be effective. Anti inflammatory and antiviral drugs that can address these genetic problems should be the focus of additional research, the researchers said.
"We found a new and very credible genetic association in covid-19 associated with critical illness," the researchers wrote. "Some of these associations directly lead to potential therapies to enhance interferon signaling, antagonize monocyte activation and infiltration into the lung, or specifically target harmful inflammatory pathways. Although this greatly increases the biological principles that support specific therapies, each treatment must be tested in large-scale clinical trials before it can be put into clinical practice. "
The full text of the study was published inNatureIn the magazine.